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American Society of Hematology, Blood, p. blood-2018-05-852798

DOI: 10.1182/blood-2018-05-852798

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Crbn I391V is sufficient to confer in vivo sensitivity to thalidomide and its derivatives in mice

Distributing this paper is prohibited by the publisher
Distributing this paper is prohibited by the publisher

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Abstract

Key Points Crbn I391V mice degrade known thalidomide derivative targets and recapitulate thalidomide-induced cytopenias and teratogenicity. Degradation of Ck1α is sufficient to explain the in vivo therapeutic window of lenalidomide in del(5q) myelodysplastic syndrome.